Endocrine Pharm

Question 1

Name the rapid acting insulin preparations

Answer 1

Lispro, Aspart, Glulisine

Question 2

MOA of insulin

Answer 2

Bind insulin receptor (tyrosine kinase activity). Liver: Increase glucose stored as glycogen. Muscle: Increase glycogen, protein synthesis. Fat: Increase TG storage. Cell membrane: Increase K+ uptake

Question 3

Adverse effects of insulin

Answer 3

Hypoglycemia, lipodystrophy, rare hypersensitivity reactions

Question 4

Short acting insulin

Answer 4

Regular insulin

Question 5

Intermediate acting insulin

Answer 5

NPH

Question 6

Long acting insulin

Answer 6

Detemir, glargine

Question 7

MOA of Amylin analogs

Answer 7

Decrease glucagon release, decrease gastric acid emptying, increase satiety

Question 8

Name the Amylin analog

Answer 8

Pramlintide

Question 9

MOA of GLP-1 analogs

Answer 9

Decrease glucagon release, decrease gastric emptying, increase glucose dependent insulin release, increase satiety

Question 10

Name the GLP-1 analogs

Answer 10

Exenatide, liragtutide

Question 11

What are adverse effects of GLP-1 analogs?

Answer 11

Nausea, vomiting, pancreatitis. Promote weight loss (often desired)

Question 12

MOA of Biguanides

Answer 12

Inhibit hepatic gluconeogenesis and the action of glucagon, by inhibiting mGPD. Increase glycolysis, peripheral glucose uptake (increase insulin sensitivity)

Question 13

What category of drugs is Metformin?

Answer 13

Biguanide

Question 14

Adverse effects of Metformin?

Answer 14

GI upset, lactic acidosis (use with caution in renal insufficiency), B12 deficiency. Promote weight loss (often desired).

Question 15

What are the 1st generation sulfonylureas?

Answer 15

Chlorpropamide, tolbutamide

Question 16

What are the 2nd generation sulfonylureas?

Answer 16

Glimepiride, glipizide, gylburide

Question 17

MOA of sulfonylureas

Answer 17

Close K+ channel in pancreatic beta cell membrane, leads to cell depolarizing, insulin release via increase Ca2+ influx

Question 18

Name the Meglitinides

Answer 18

Nateglinide, repaglinide

Question 19

MOA of meglitinides

Answer 19

Close K+ channel in pancreatic beta cell membrane, leads to cell depolarizing, insulin release via increase Ca2+ influx (binding site differs from sulfonylureas)

Question 20

Name the DPP-4 inhibitors

Answer 20

Linagliptin, saxagliptin, sitagliptin

Question 21

MOA of DPP-4 inhibitors

Answer 21

Inhibit DPP-4 enzyme that deactivates GLP-1. Decrease glucagon release, gastric emptying. Increase glucose-dependent insulin release, satiety.

Question 22

Side effects of DPP-4 inhibitors

Answer 22

Mild urinary or respiratory infections, weight neutral

Question 23

Name the Glitazones/thiazolidinediones

Answer 23

Pioglitazone, rosiglitazone

Question 24

MOA of glitazones/thiazolidinediones

Answer 24

Binds to PPAR-gamma nuclear transcription regulator, which increases insulin sensitivity and levels of adiponectin, leads to regulation of glucose metabolism and fatty acid storage

Question 25

Adverse effects of glitazones/thiazolidinediones

Answer 25

Weight gain, edema, HF, increased risk of fractures. Delated onset of action (several weeks). Not used in HF pts

Question 26

Name the SGLT2 inhibitors

Answer 26

Canagliflozin, dapagliflozin, empagliflozin

Question 27

MOA of SGLT2 inhibitors

Answer 27

Block reabsorption of glucose in proximal convoluted tubule

Question 28

Adverse effects of SGLT2 inhibitors

Answer 28

Glucosuria, UTIs, vaginal yeast infections, hyperkalemia, dehydration, weight loss

Question 29

Name the alpha-glucosidase inhibitors

Answer 29

Acarbose, miglitol

Question 30

MOA of alpha-glucosidase inhibitors

Answer 30

Inhibit intestinal brush border alpha-glucosidases, leads to delayed carbohydrate hydrolysis and glucose absorption, which leads to decreased postprandial hyperglycemia

Question 31

Name the Thioamides

Answer 31

Propylthiouricil, methimazole

Question 32

MOA of Thioamides

Answer 32

Block thyroid peroxidase, inhibiting the oxidation of iodine and the organification and coupling of iodine, leading to inhibition of thyroid hormone synthesis.
PTU also blocks 5’-deiodinase and leads to decreased peripheral converstion of T4 to T3.

Question 33

Clinical use of Thioamides

Answer 33

Hyperthyroidism

Question 34

Adverse effects of Thioamides

Answer 34

Skin rash, agranulocytosis (rare), aplastic anemia, hepatotoxicity.

Question 35

What can Methimazole cause if taken during pregnancy?

Answer 35

Aplasia cutis

Question 36

Clinical use of ADH antagonists

Answer 36

SIADH, block action of ADH at V2-receptor

Question 37

Clinical use of Desmopressin

Answer 37

Central (not nephrogenic) DI, von Willebrand disease, sleep enuresis, hemophilia A

Question 38

GH clinical uses

Answer 38

GH deficiency, Turner syndrome

Question 39

Oxytocin clinical uses

Answer 39

Labor induction, milk letdown; controls uterine hemorrhage

Question 40

Somatostatin (octreotide) clinical uses

Answer 40

Acromegaly, carcinoid syndrome, gastrinoma, glucagonoma, esophageal varices

Question 41

MOA of Demeclocycline

Answer 41

ADH antagonist

Question 42

Clinical use of Demeclocycline

Answer 42

SIADH

Question 43

MOA of Fludrocortisone

Answer 43

Synthetic analog of aldosterone with little glucocorticoid effects

Question 44

Clinical use of Fludrocortisone

Answer 44

Mineralocorticoid replacement in primary adrenal insufficiency

Question 45

MOA of Cinacalcet

Answer 45

Sensitizes Ca2+-sensing receptors (CaSR) in parathyroid gland to circulating Ca2+, leading to decreased PTH

Question 46

Clinical use of Cinacalcet

Answer 46

Refractory hypercalcemia in primary hyperparathyroidism, secondary hyperparathyroidism, or parathyroid carcinoma

Question 47

MOA of Sevelamer

Answer 47

Nonabsorable phosphate binder that prevents phosphate absorption from the GI tract

Question 48

Clinical use of Sevelamer

Answer 48

Hyperphosphatemia in CKD